CCAMLR is a commission of 36 nations founded in 1982 to protect Antarctica and preserve this continent for science and future generations. This monumental agreement is all the more remarkable when you consider the size of Antarctica (larger than the USA) and the lousy state of the year 1982 (height of Reagan and AIDS). This commission has largely succeeded in protecting Antarctica from mining and harvesting operations. It has allowed the National Science Foundation (backed by unobtrusive US military forces) to largely administer access for biology, geology, and climate science.

But off the coast, it’s been another story, with fishing and whaling threatening the ecosystems of the Southern Ocean. This week, however, CCAMLR has reached agreement to put off limits an enormous swath of ocean known as the Ross Sea.

The Ross Sea is familiar as the region I crossed in the C-17 cargo hold on our way to McMurdo Station. McMurdo sits on the lava spit of Ross Island; in the above map, located at the edge of the ice shelf just below the words “Ross Sea Shelf.” The edge of the ice shelf is a magical region attracting thousands of penguins, seals and killer whales. On our final helicopter flight back from Taylor Valley, the pilot dipped and buzzed the shelf, startling pods of Adelies, Emperors and others for our last good look. The new CCAMLR agreement will protect more than a million and a half square kilometers of this ecosystem.

Meanwhile, back at Kenyon our own bit of Antarctica in our -80 freezer is yielding up secrets to the science of our supercomputer. Current projects include:

Discovering life forms capable of living half the year at forty below (where centigrade equals Fahrenheit)

Mining the microbial genomes for enzymes that make new antibiotics

Growing purple bacteria that store sunlight as hydrogen fuel–a stowaway colony from the mat stuff we picked up off the ice.

Usually we look for antibiotics in exotic places such as Antarctica, aiming to find new drugs that no human pathogen has ever seen. But what if an antibiotic could be hiding in plain sight–or nearer yet, up your nose?

That’s what Alexander Zipperer and colleagues found, at the University of Tübingen. They focused on a pathogen Staphylococcus aureus, cause of serious skin infections including drug-resistant varieties such as methicillin-resistant Staph (MRSA). But S. aureus has a surprising ability to hang out up the nose of healthy, unsuspecting carriers–that’s about one in three of us. Look to your right, then your left: One of you three’s got it.

So what keeps some of us healthy, despite this pathogen? The German researchers proposed there might exist some other nose-loving bacterium, part of our nasal snot microbiome–some bacterium that defends us from the bad ones. To find this white-knight defender, the researchers screened a collection of previously isolated nasal bacteria, cultured on a synthetic nasal medium (i.e. standardized snot). They tested individual isolates by dropping each culture upon a lawn of the tester strain Staph aureus. One isolate Staphylococcus lugdunensis showed a clear halo, a region where the tester Staph failed to grow.

The new S. lugdunensis was shown to produce a novel antibiotic, which they named lugdunin. Lugdunin (above) is a nonribosomal peptide; like vancomycin, the antibiotic is formed by a factory-modular enzyme that generates peptide bonds. Unlike ribosomal proteins, however, the nonribosomal peptide can contain all kinds of amino acids, beyond the canonical twenty. Lugdunin actually includes a thiazolidine, a unique five-membered ring including a sulfur atom.

So we may have a new antibiotic; or even a new probiotic, in the form of S. lugdunensis to inoculate our noses.

The Tasmanian Devil is today’s largest known marsupial mammal; which is not saying much, barely two feet long aside from tail. Hunted to extinction, these tiny fierce predators remain today on the island of Tasmania. They form extended social networks, fighting, mating, and eating entire carcasses down to the bone–a tidy habit that actually endears them to Tasmanian farmers. Considered an iconic symbol and attractor of tourists to Tasmania, the devil now enjoys the benefits of the Australian government’s Save the Tasmanian Devil Program.

Like most charismatic mammals, the devil’s main enemy for survival has long been considered the humans who hunted them to near extinction. But in recent years, devils face an even more horrible foe: transmissible facial tumors, known as devil facial tumor disease (DFTD). First seen in 1996, the tumors disfigure the face in horrible ways that I prefer not to show here, but you can find them all over the internet. What is unusual about these tumors is that the cancerous tissue actually transmits like a pathogen to other animals, typically during fighting, which the little carnivores spend a lot of time doing. Why does the cancer spread? Apparently because the devil populations have such low diversity that their immune systems fail to recognize the tumor cells as foreign. The tumor spreads so fast that most devils get infected and eventually die of organ failure or starvation. Overall the population has declined by 90%.

Will the devil go extinct? Surprisingly, the answer appears to be no. A new study by an international research team, including Brendan Epstein and Andrew Storfer from Washington State U, focuses on a few isolated populations of devils that seem to be holding their own (pink disks below). This map (Figure 1) shows the steady advance of the disease across Tasmania, and the sites of surviving populations.

The authors of the study reasoned that any devil populations having survived the near-100% fatality rate of DFTD must have undergone selection for specific gene mutations that confer resistance to the tumors. Sure enough, the animals’ sequenced genomes reveal fascinating mutations.

In the genomes, seven DNA regions were found that showed high frequency for particular alleles (variant versions of a gene). These regions are “known to science” because they share similarity with the DNA of all mammals, who share a common ancestor. Five of these seven regions encode proteins that are associated with cancer prevention or the immune system, as studies in other mammals. For example, protein CD146 is known as “melanoma adhesion molecule.” This protein functions in normal cell cycle and adhesion (attachment to other cells) as well as regulation of the immune system that prevents cancer. Another protein is known as a “proto-oncogene,” that is, a gene that can mutate to cancer–but ordinarily protects from cancer. Presumably, the mutant version of these proteins somehow protects the individual devils from the tumors that came close to exterminating them.

The authors title their work, “Rapid Evolutionary Response to a Transmissible Cancer in Tasmanian Devils.” The case shows an unusually sped up version of the evolutionary arms race that faces all living things; how to out-live that which threatens survival and reproduction. The recent finding is good news for devils–and may also shed light on cancer prevention in related species, including our own.

According to authors in the journal Science, experiments demonstrate the ability of newly hatched duckling to distinguish the concepts “same” and “different.”

Previously, the authors note, “pigeons and bees can be trained to discriminate whether novel images contain humans or not, or whether novel paintings are by Monet or Picasso.” Such discrimination requires extensive training between specific patterns–the pattern of a “human” shape, versus other; or the patterns of Monet versus Picasso. The discrimination of paintings does not imply artistic talent; in fact, the animals might be observing something trivial, such as the color scheme or size of objects depicted. These previous findings all required concrete objects to discriminate.

But can we demonstrate learning of an abstract concept?

Authors Antone Martinho III and Alex Kacelnik, of the Oxford Zoology department, claim to have done just that. They made ingenious use of a powerful memory tool: the imprinting of birds on their parent. Imprinting has long been demonstrated as an introductory lab in biology. The student waits for a duck egg to hatch; then the first thing the hatchling sees or hears is the student. Forever after, the hatchling follows the student as if they were its mother.

If ducklings can imprint upon a human student, what about inanimate objects? Or even an abstract concept?

In the experiment, newly hatched ducklings were exposed to pairs of objects.

In some cases, the hatchlings were exposed to pairs of objects that were identical. Other hatchlings were presented with pairs of objects that differed in shape or color.

After exposure, the hatchlings were then presented with a pair of objects of a different kind (balls versus cones). But two kinds of presentation were done: of two different objects, or two identical objects. For example, a duck was imprinted on “two spheres”, then tested on “two cones” (identical) or on “cube plus tower” (different). The duck’s preference was then measured by the number of times it stepped toward the object pair. Even though the new objects were of a different kind, the ducks still preferred (stepped toward) an identical pair, if it had imprinted on an identical pair; or a dissimilar pair, if it had imprinted on a dissimilar pair. The experiment worked either for shape or color.

When picked up by the canonical alien abductors, I wonder how many of us humans could pass this test.

The Peckham society is a treasure trove of fascinating and diverse spider behavior, such as this one feasting on a fellow spider. Not the same species, so it doesn’t count as cannibalism (unless you’re a cannibal for eating a cow.)

And for the truly insatiable spider enthusiast, check out the Peckham’s video collection. To think that all this variety represents one small branch of the arachnid tree–It’s enough to give some hope for Earth’s biological world.

Beach time of year, as good a time as any to wonder how fast the ocean is rising. In the long run, we’re locked into several feet of rise in the next century, possibly more if Antarctic glaciers accelerate.

This great figure from Discover Magazine shows how undersea “rivers” are undermining the ice shelves, accelerating their fall in unpredictable ways.

But in the near term, the ocean’s movements look surprisingly complex–giving naysayers excuses to deny the problem. For instance, the sea levels right around Antarctica will actually fall, relative to the Antarctic land mass. This happens because the mass of ice will be gone, and thus there will be less gravitational pull on the water. In addition, the land will “spring up” slightly, like the couch cushion when you get up for a snack. The net result, though, is water rising faster in farther off places like Florida and New York.

Another place ocean levels are falling is west of Mexico. The reason is weather patterns, a cyclical pattern called the Pacific Decadal Oscillation. This pattern, which takes higher math to understand, results in a decade of cooler water in the Pacific, which means denser water and lower sea level. Of course in the following period, the sea will rise double, making up for lost time.

It is old news that exercise improves the brain–at any age, from children who walk to school, to the elderly who garden. Prolonged exercise, as in running, is what we evolved to do. Running–and the intellect involved to track down animals–led early humans into a unique form of hunting, one that required memory and calculation. But what is the physiological connection? How do the heart and skeletal muscles affect the brain?

The researchers set mice to running on their proverbial running wheels. After thirty days running, compared with slacker mice, the runners showed increased amounts of a brain protein called BDNF. BDNF is a protein that encourages nerves to grow; a member of the same family as nerve growth factor, the protein discovered by the famous Nobel laureate Rita Levi-Montalcini (who makes an appearance in The Highest Frontier). BDNF helps maintain synapses and grows new ones in the hippocampus, cortex and forebrain; basically everywhere needed for higher function.

So what is the molecular mechanism? The authors proposed and tested a form of “epigenetics,” a mechanism by which environmental experience alters chemical tags attached to the neurons’s DNA, or to histone proteins associated with the DNA. Epigenetic markers involve enzymes called histone deacetylases (HDAC). The HDAC removes an acetyl group from a histone, a binding protein that helps “pack” DNA and determines whether its gene gets transcribed to RNA. Here, DNA is wrapped two turns around a core of eight histones (colored).

The authors did experiments that showed that inhibitors of HDAC proteins (specifically HDAC2 and HDAC3) could prevent the histone deacetylation, leaving the DNA wrapped around histones marked with acetyl groups. Acetyl groups usually code for “go ahead” and transcribe a gene. So now the gene encoding BDNF goes ahead and gets transcribed to RNA, which then gets translated by ribosomes to make BDNF protein.

What all does this have to do with mice on their running wheels? The running mice make extra ketone bodies such as D-β-hydroxybutyrate (DBHB). Ketone bodies get made by your liver after intense exercise uses up carbohydrates. Excess ketone bodies can cause problems, but as a short-term response to exercise they supercharge the brain. In particular, DBHB blocks production of HDAC2 and HDAC3 (that is what the cross-blocked vertical lines mean, in the diagram above). Since DBHB blocks the HDACs, and the HDACs block expression of BDNF, the net result is that ketone bodies induce BDNF which enhances neurons and makes more synapses.